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Article ; Online: Editorial

Yuji Nozaki / Poh-Yi Gan / Joshua Daniel Ooi

Frontiers in Medicine, Vol

The Network of Inflammatory Mechanisms in Kidney Disease: Mechanism and New Therapeutic Agents

2021 Volume 8

Keywords	therapeutic agents ; kidney disease ; autoimmune disease ; cytokines ; signaling pathways ; Medicine (General) ; R5-920
Language	English
Publishing date	2021-12-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Editorial: The Network of Inflammatory Mechanisms in Kidney Disease: Mechanism and New Therapeutic Agents.

Nozaki, Yuji / Gan, Poh-Yi / Ooi, Joshua Daniel

Frontiers in medicine

2021 Volume 8, Page(s) 799850

Language	English
Publishing date	2021-12-09
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2021.799850
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Article ; Online: Angiopep-2-Functionalized Lipid Cubosomes for Blood-Brain Barrier Crossing and Glioblastoma Treatment.

Cai, Xudong / Refaat, Ahmed / Gan, Poh-Yi / Fan, Bo / Yu, Haitao / Thang, San H / Drummond, Calum J / Voelcker, Nicolas H / Tran, Nhiem / Zhai, Jiali

ACS applied materials & interfaces

2024 Volume 16, Issue 10, Page(s) 12161–12174

Abstract: Glioblastoma multiforme (GBM) is an aggressive brain cancer with high malignancy and resistance to conventional treatments, resulting in a bleak prognosis. Nanoparticles offer a way to cross the blood-brain barrier (BBB) and deliver precise therapies to ... ...

Abstract	Glioblastoma multiforme (GBM) is an aggressive brain cancer with high malignancy and resistance to conventional treatments, resulting in a bleak prognosis. Nanoparticles offer a way to cross the blood-brain barrier (BBB) and deliver precise therapies to tumor sites with reduced side effects. In this study, we developed angiopep-2 (Ang2)-functionalized lipid cubosomes loaded with cisplatin (CDDP) and temozolomide (TMZ) for crossing the BBB and providing targeted glioblastoma therapy. Developed lipid cubosomes showed a particle size of around 300 nm and possessed an internal ordered inverse primitive cubic phase, a high conjugation efficiency of Ang2 to the particle surface, and an encapsulation efficiency of more than 70% of CDDP and TMZ.
MeSH term(s)	Humans ; Glioblastoma/drug therapy ; Glioblastoma/pathology ; Blood-Brain Barrier/pathology ; Tissue Distribution ; Prospective Studies ; Cell Line, Tumor ; Temozolomide ; Brain Neoplasms/pathology ; Nanoparticles/therapeutic use ; Lipids/therapeutic use ; Peptides
Chemical Substances	Angiopep-2 ; Temozolomide (YF1K15M17Y) ; Lipids ; Peptides
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Journal Article
ISSN	1944-8252
ISSN (online)	1944-8252
DOI	10.1021/acsami.3c14709
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Article ; Online: Cytokines: Names and Numbers You Should Care About.

Holdsworth, Stephen R / Gan, Poh-Yi

Clinical journal of the American Society of Nephrology : CJASN

2015 Volume 10, Issue 12, Page(s) 2243–2254

Abstract: Cytokines play an important role in host defense against microorganisms. They orchestrate innate immunity by inducing protective local inflammation and systemic acute phase responses. Cytokines are important in initiating, amplifying, directing, ... ...

Abstract	Cytokines play an important role in host defense against microorganisms. They orchestrate innate immunity by inducing protective local inflammation and systemic acute phase responses. Cytokines are important in initiating, amplifying, directing, mediating, and regulating adaptive immunity. Unfortunately, they may also direct tissue damage if excessive responses occur or if they are involved in directing and mediating autoimmunity. Under these circumstances, cytokines are potential therapeutic targets. Over the last 20 years, we have seen the successful development and clinical implementation of biologic strategies that target key cytokines in specific inflammatory diseases with efficacy, specificity, and toxicity profiles challenging conventional drug therapies. These therapies are finding new applications and many new agents show promise. Unfortunately, these new cytokine-based therapies have had little effect on renal disease. This review provides evidence that common renal diseases, including those causing AKI and the autoimmune proliferative and crescentic forms of GN, have cytokine mediation profiles that suggest they would be susceptible to cytokine-targeting therapeutic strategies.
MeSH term(s)	Acute Kidney Injury/diagnosis ; Acute Kidney Injury/drug therapy ; Acute Kidney Injury/genetics ; Acute Kidney Injury/immunology ; Acute Kidney Injury/metabolism ; Adaptive Immunity ; Animals ; Anti-Inflammatory Agents/therapeutic use ; Autoimmunity ; Cytokines/antagonists & inhibitors ; Cytokines/genetics ; Cytokines/immunology ; Cytokines/metabolism ; Cytokines/therapeutic use ; Genetic Therapy/methods ; Glomerulonephritis/diagnosis ; Glomerulonephritis/drug therapy ; Glomerulonephritis/genetics ; Glomerulonephritis/immunology ; Glomerulonephritis/metabolism ; Humans ; Immunity, Innate ; Immunologic Factors/therapeutic use ; Molecular Targeted Therapy ; Signal Transduction
Chemical Substances	Anti-Inflammatory Agents ; Cytokines ; Immunologic Factors
Language	English
Publishing date	2015-12-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.07590714
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Article: Supervised machine learning for semi-quantification of extracellular dna in glomerulonephritis

O'Sullivan, Kim Maree / Creed, Sarah / Gan, Poh-Yi / Holdsworth, Stephen R

Journal of visualized experiments. 2020 June 18, , no. 160

2020

Abstract: Glomerular cell death is a pathological feature of myeloperoxidase anti neutrophil cytoplasmic antibody associated vasculitis (MPO-AAV). Extracellular deoxyribonucleic acid (ecDNA) is released during different forms of cell death including apoptosis, ... ...

Abstract	Glomerular cell death is a pathological feature of myeloperoxidase anti neutrophil cytoplasmic antibody associated vasculitis (MPO-AAV). Extracellular deoxyribonucleic acid (ecDNA) is released during different forms of cell death including apoptosis, necrosis, necroptosis, neutrophil extracellular traps (NETs) and pyroptosis. Measurement of this cell death is time consuming with several different biomarkers required to identify the different biochemical forms of cell death. Measurement of ecDNA is generally conducted in serum and urine as a surrogate for renal damage, not in the actual target organ where the pathological injury occurs. The current difficulty in investigating ecDNA in the kidney is the lack of methods for formalin fixed paraffin embedded tissue (FFPE) both experimentally and in archived human kidney biopsies. This protocol provides a summary of the steps required to stain for ecDNA in FFPE tissue (both human and murine), quench autofluorescence and measure the ecDNA in the resulting images using a machine learning tool from the publicly available open source ImageJ plugin trainable Weka segmentation. Trainable Weka segmentation is applied to ecDNA within the glomeruli where the program learns to classify ecDNA. This classifier is applied to subsequent acquired kidney images, reducing the need for manual annotations of each individual image. The adaptability of the trainable Weka segmentation is demonstrated further in kidney tissue from experimental murine anti-MPO glomerulonephritis (GN), to identify NETs and ecMPO, common pathological contributors to anti-MPO GN. This method provides objective analysis of ecDNA in kidney tissue that demonstrates clearly the efficacy in which the trainable Weka segmentation program can distinguish ecDNA between healthy normal kidney tissue and diseased kidney tissue. This protocol can easily be adapted to identify ecDNA, NETs and ecMPO in other organs.
Keywords	DNA ; antibodies ; artificial intelligence ; biomarkers ; biopsy ; blood serum ; formalin ; glomerulonephritis ; humans ; kidneys ; mice ; myeloperoxidase ; necroptosis ; necrosis ; neutrophils ; pyroptosis ; urine ; vasculitis
Language	English
Dates of publication	2020-0618
Size	p. e61180.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/61180
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Supervised Machine Learning for Semi-Quantification of Extracellular DNA in Glomerulonephritis.

O'Sullivan, Kim Maree / Creed, Sarah / Gan, Poh-Yi / Holdsworth, Stephen R

Journal of visualized experiments : JoVE

2020 , Issue 160

Abstract	Glomerular cell death is a pathological feature of myeloperoxidase anti neutrophil cytoplasmic antibody associated vasculitis (MPO-AAV). Extracellular deoxyribonucleic acid (ecDNA) is released during different forms of cell death including apoptosis, necrosis, necroptosis, neutrophil extracellular traps (NETs) and pyroptosis. Measurement of this cell death is time consuming with several different biomarkers required to identify the different biochemical forms of cell death. Measurement of ecDNA is generally conducted in serum and urine as a surrogate for renal damage, not in the actual target organ where the pathological injury occurs. The current difficulty in investigating ecDNA in the kidney is the lack of methods for formalin fixed paraffin embedded tissue (FFPE) both experimentally and in archived human kidney biopsies. This protocol provides a summary of the steps required to stain for ecDNA in FFPE tissue (both human and murine), quench autofluorescence and measure the ecDNA in the resulting images using a machine learning tool from the publicly available open source ImageJ plugin trainable Weka segmentation. Trainable Weka segmentation is applied to ecDNA within the glomeruli where the program learns to classify ecDNA. This classifier is applied to subsequent acquired kidney images, reducing the need for manual annotations of each individual image. The adaptability of the trainable Weka segmentation is demonstrated further in kidney tissue from experimental murine anti-MPO glomerulonephritis (GN), to identify NETs and ecMPO, common pathological contributors to anti-MPO GN. This method provides objective analysis of ecDNA in kidney tissue that demonstrates clearly the efficacy in which the trainable Weka segmentation program can distinguish ecDNA between healthy normal kidney tissue and diseased kidney tissue. This protocol can easily be adapted to identify ecDNA, NETs and ecMPO in other organs.
MeSH term(s)	Animals ; Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/blood ; Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/immunology ; Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/pathology ; Biopsy ; DNA/analysis ; Extracellular Space/metabolism ; Extracellular Traps/metabolism ; Glomerulonephritis/genetics ; Humans ; Image Processing, Computer-Assisted ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Male ; Mice, Inbred C57BL ; Models, Biological ; Peroxidase/metabolism ; Supervised Machine Learning
Chemical Substances	DNA (9007-49-2) ; Peroxidase (EC 1.11.1.7)
Language	English
Publishing date	2020-06-18
Publishing country	United States
Document type	Journal Article ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/61180
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Article ; Online: Heterologous Immunity Between SARS-CoV-2 and Pathogenic Bacteria.

Eggenhuizen, Peter J / Ng, Boaz H / Chang, Janet / Cheong, Rachel M Y / Yellapragada, Anusha / Wong, Wey Y / Ting, Yi Tian / Monk, Julie A / Gan, Poh-Yi / Holdsworth, Stephen R / Ooi, Joshua D

Frontiers in immunology

2022 Volume 13, Page(s) 821595

Abstract: Heterologous immunity, when the memory T cell response elicited by one pathogen recognizes another pathogen, has been offered as a contributing factor for the high variability in coronavirus disease 2019 (COVID-19) severity outcomes. Here we demonstrate ... ...

Abstract	Heterologous immunity, when the memory T cell response elicited by one pathogen recognizes another pathogen, has been offered as a contributing factor for the high variability in coronavirus disease 2019 (COVID-19) severity outcomes. Here we demonstrate that sensitization with bacterial peptides can induce heterologous immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) derived peptides and that vaccination with the SARS-CoV-2 spike protein can induce heterologous immunity to bacterial peptides. Using
MeSH term(s)	Adult ; Bacterial Infections/immunology ; COVID-19/immunology ; COVID-19 Vaccines/immunology ; Cells, Cultured ; Coculture Techniques ; Female ; Humans ; Immunity, Cellular/immunology ; Immunity, Heterologous/immunology ; Male ; SARS-CoV-2/immunology ; Spike Glycoprotein, Coronavirus/immunology ; T-Lymphocytes/immunology
Chemical Substances	COVID-19 Vaccines ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
Language	English
Publishing date	2022-01-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.821595
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Article ; Online: The C3aR promotes macrophage infiltration and regulates ANCA production but does not affect glomerular injury in experimental anti-myeloperoxidase glomerulonephritis.

Dick, Jonathan / Gan, Poh-Yi / Kitching, A Richard / Holdsworth, Stephen R

PloS one

2018 Volume 13, Issue 1, Page(s) e0190655

Abstract: The anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitides are autoimmune diseases associated with significant morbidity and mortality. They often affect the kidney causing rapidly progressive glomerulonephritis. While signalling by ... ...

Abstract	The anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitides are autoimmune diseases associated with significant morbidity and mortality. They often affect the kidney causing rapidly progressive glomerulonephritis. While signalling by complement anaphylatoxin C5a though the C5a receptor is important in this disease, the role of the anaphylatoxin C3a signalling via the C3a receptor (C3aR) is not known. Using two different murine models of anti-myeloperoxidase (MPO) glomerulonephritis, one mediated by passive transfer of anti-MPO antibodies, the other by cell-mediated immunity, we found that the C3aR did not alter histological disease severity. However, it promoted macrophage recruitment to the inflamed glomerulus and inhibited the generation of MPO-ANCA whilst not influencing T cell autoimmunity. Thus, whilst the C3aR modulates some elements of disease pathogenesis, overall it is not critical in effector responses and glomerular injury caused by autoimmunity to MPO.
MeSH term(s)	Animals ; Antibodies, Antineutrophil Cytoplasmic/immunology ; Antibody Formation ; Autoimmunity ; Complement C3a/metabolism ; Glomerulonephritis/immunology ; Glomerulonephritis/pathology ; Immunity, Cellular ; Macrophages/pathology ; Mice ; Mice, Inbred C57BL ; Peroxidase/immunology ; Receptors, Complement/metabolism ; Receptors, Complement/physiology
Chemical Substances	Antibodies, Antineutrophil Cytoplasmic ; Receptors, Complement ; Complement C3a (80295-42-7) ; Peroxidase (EC 1.11.1.7)
Language	English
Publishing date	2018-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0190655
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Article ; Online: The C3aR promotes macrophage infiltration and regulates ANCA production but does not affect glomerular injury in experimental anti-myeloperoxidase glomerulonephritis.

Jonathan Dick / Poh-Yi Gan / A Richard Kitching / Stephen R Holdsworth

PLoS ONE, Vol 13, Iss 1, p e

2018 Volume 0190655

Abstract	The anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitides are autoimmune diseases associated with significant morbidity and mortality. They often affect the kidney causing rapidly progressive glomerulonephritis. While signalling by complement anaphylatoxin C5a though the C5a receptor is important in this disease, the role of the anaphylatoxin C3a signalling via the C3a receptor (C3aR) is not known. Using two different murine models of anti-myeloperoxidase (MPO) glomerulonephritis, one mediated by passive transfer of anti-MPO antibodies, the other by cell-mediated immunity, we found that the C3aR did not alter histological disease severity. However, it promoted macrophage recruitment to the inflamed glomerulus and inhibited the generation of MPO-ANCA whilst not influencing T cell autoimmunity. Thus, whilst the C3aR modulates some elements of disease pathogenesis, overall it is not critical in effector responses and glomerular injury caused by autoimmunity to MPO.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2018-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Biologics for the treatment of autoimmune renal diseases.

Holdsworth, Stephen R / Gan, Poh-Yi / Kitching, A Richard

Nature reviews. Nephrology

2016 Volume 12, Issue 4, Page(s) 217–231

Abstract: Biological therapeutics (biologics) that target autoimmune responses and inflammatory injury pathways have a marked beneficial impact on the management of many chronic diseases, including rheumatoid arthritis, psoriasis, inflammatory bowel disease, and ... ...

Abstract	Biological therapeutics (biologics) that target autoimmune responses and inflammatory injury pathways have a marked beneficial impact on the management of many chronic diseases, including rheumatoid arthritis, psoriasis, inflammatory bowel disease, and ankylosing spondylitis. Accumulating data suggest that a growing number of renal diseases result from autoimmune injury - including lupus nephritis, IgA nephropathy, anti-neutrophil cytoplasmic antibody-associated glomerulonephritis, autoimmune (formerly idiopathic) membranous nephropathy, anti-glomerular basement membrane glomerulonephritis, and C3 nephropathy - and one can speculate that biologics might also be applicable to these diseases. As many autoimmune renal diseases are relatively uncommon, with long natural histories and diverse outcomes, clinical trials that aim to validate potentially useful biologics are difficult to design and/or perform. Some excellent consortia are undertaking cohort studies and clinical trials, but more multicentre international collaborations are needed to advance the introduction of new biologics to patients with autoimmune renal disorders. This Review discusses the key molecules that direct injurious inflammation and the biologics that are available to modulate them. The opportunities and challenges for the introduction of relevant biologics into treatment protocols for autoimmune renal diseases are also discussed.
MeSH term(s)	Anti-Glomerular Basement Membrane Disease/drug therapy ; Anti-Glomerular Basement Membrane Disease/immunology ; Autoimmune Diseases/drug therapy ; Autoimmune Diseases/immunology ; Biological Products/therapeutic use ; Glomerulonephritis, IGA/drug therapy ; Glomerulonephritis, IGA/immunology ; Glomerulonephritis, Membranous/drug therapy ; Glomerulonephritis, Membranous/immunology ; Humans ; Immunologic Factors/therapeutic use ; Kidney Diseases/drug therapy ; Kidney Diseases/immunology ; Lupus Nephritis/drug therapy ; Lupus Nephritis/immunology
Chemical Substances	Biological Products ; Immunologic Factors
Language	English
Publishing date	2016-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/nrneph.2016.18
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